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Related Experiment Videos

Endogenous basal nitric oxide production does not control myocardial oxygen consumption or function

J D Sadoff1, P M Scholz, H R Weiss

  • 1Department of Surgery, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick 08903-0019, USA.

Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
|April 1, 1996
PubMed
Summary

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Endogenous nitric oxide (NO) production in the heart does not appear to affect myocardial oxygen consumption or function. Inhibiting NO synthase with L-NAME and L-NMMA caused vasoconstriction but no changes in cardiac work or energy use.

Area of Science:

  • Cardiovascular Physiology
  • Biochemistry

Background:

  • Previous studies demonstrated exogenous nitric oxide (NO) donors induce vasodilation and negative inotropy via guanylate cyclase activation and cyclic GMP increase.
  • The role of endogenous myocardial NO production in regulating myocardial oxygen consumption and cardiac function in vivo remained unclear.

Purpose of the Study:

  • To test the hypothesis that endogenous myocardial NO production limits myocardial oxygen consumption and function in vivo.
  • To investigate the effects of NO synthase inhibition on coronary blood flow, myocardial oxygen consumption, cardiac work, and cyclic GMP levels.

Main Methods:

  • Utilized NO synthase inhibitors N(G)-nitro-L-arginine methyl ester (L-NAME) and N(G)-monomethyl-L-arginine (L-NMMA) in anesthetized dogs.
  • Administered inhibitors into the left anterior descending coronary artery (LAD), with the circumflex (CFX) artery serving as a control.

Related Experiment Videos

  • Measured regional segment work, local myocardial O2 consumption, and myocardial cyclic GMP levels.

    • Main Results:

    • L-NAME and L-NMMA induced local coronary vasoconstriction and increased O2 extraction.
    • No significant changes were observed in local myocardial O2 consumption, segment force, percent shortening, or segment work.
    • Myocardial cyclic GMP levels remained comparable between the LAD and control regions.

    Conclusions:

    • Blockade of endogenous NO production with L-NAME and L-NMMA effectively causes cardiac vasoconstriction in anesthetized dogs.
    • The administered doses of NO synthase inhibitors did not alter local myocardial function, oxygen consumption, or cyclic GMP levels.